High dietary vitamin A (retinyl palmitate) and cellular immune functions in mice


Moriguchi S






High dietary intakes (4000-650,000 IU/kg diet) of vitamin A (retinyl palmitate, RP) modified the functions of peritoneal macrophages (PM). The number of peritoneal exudated cells (PEC) obtained from CD-1 mice increased significantly at both 7 and 10 weeks after initiation of the RP diets. The percentage of PM in PEC showed no significant difference between dietary groups and was at levels of 55-60%. PM from mice fed high RP diets showed higher tumoricidal activities than PM from controls without any preincubation with macrophage activators. Enhancement of in vitro tumoricidal activity of PM increased with increasing contents of RP in the diets, reaching 30% lysis by PM isolated from mice fed the highest RP (650,000 IU/kg diet) diet. However, the in vitro activation of tumoricidal ability of PM by macrophage-activating factor (MAF) was inversely correlated with the dietary RP content. The tumoricidal activities of PM from mice fed the highest RP diet were not enhanced by MAF. However, these PM showed an increased ability to phagocytose SRBC and opsonized SRBC compared to controls. Splenocytes and thymocytes were incubated with [3H]thymidine immediately after isolation and their mitogenic activities were measured. Splenocytes, but not thymocytes, isolated from mice fed the highest RP diet had increased mitogenesis. On the other hand, NK activity was not affected by dietary RP intake. There was a similar lysis of target cells by both splenocytes and thymocytes from mice fed diets with various RP levels. IL-1 was produced from PM by incubation with LPS, and its production was assessed using the proliferation of normal mice thymocytes. Production of IL-1 in vitro showed about a two-fold increase using cells from mice fed the highest RP diet compared to controls. High RP diets induced increased phagocytic ability and tumoricidal activity of PM but did not enhance NK activity. These findings suggest that high RP diet may cause activation of PM.

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